FINAL neuro Flashcards
What is CN IV (name, sensory vs. motor function)
Trochlear, motor
Function of CN IV
Superior oblique muscle of the eye
How is CN IV tested?
With CNIII- tracking moving objects
What is CN V (name, sensory vs. motor function)
Trigeminal, both sensory and motor
Function of CN V
Sensory signals from face (mouth, nose, eye, dura mater)
Motor fibers to the muscles of mastication
Name and briefly describe a condition causing dysfunction of CN V
Trigeminal neuralgia- hypersensitivity to pain in the areas innervated by CN V (ipsilateral face- eye, maxilla, mandible) caused by neurovascular or other compression or demyelination of CN V.
Herpes zoster opthalmicus- shingles in the opthalmic branch of trigeminal nerve
What is CN VI (name, sensory vs motor function)
Abducens, motor
Function of CN VI
motor- innervates lateral rectus of the eye
Dysfunction of CN VI causes?
Inability to ABDduct eye
Name all 12 cranial nerves
OOOTTAFVGVAH
olfactory, optic, oculomotor, trochlea, trigeminal, abducens, facial, vestibulocochlear, glossopharyngeal, vagus, accessory, hypoglossal
What is myasthenia gravis?
A chronic autoimmune disease affecting the neuromuscular junction characterized by weakness of voluntary muscles
Describe the epidemiology of myasthenia gravis
2 peaks- women in 20-30s, men in 60-60s.
Risk factors: frequently manifests for first time in pregnancy, exposure to anesthetic agents, thymic hyperplasia/ tumor, other autoimmune disorders
Time course of myasthenia gravis
insidious onset, relapse and remissions with gradual progression of disease.
What muscles are usually affected first in myasthenia graviS?
mouth, eyes, face, mouth, throat, neck
Classic triad: ptosis, diplopia, dysphagia
Describe patho of myasthenia gravis
Chronic autoimmune disorder: antibody mediated attack on acetylcholine receptors (the nicotinic receptor) at the post synaptic membrane of the neuromuscular junction. Decreased in these receptors= diminished transmission of nerve impulses across neuromuscular junction.
type 2 hypersensitivity reaction
T-cell mediated
Symptoms of myasthenia gravis
Classic triad: ptosis, diplopia, dysphagia
-difficulty chewing, drooling, slurred speech, easily fatigable, symptoms more pronounced with fatigue or in the evening
-normal sensory perception, pupillary response, coordination
-eye movement dysfunction, cannot sustain arm raise, change in voice when counting to 100
What is myasthenic crisis
Life threatening, risk of respiratory arrest, triggered when resp muscles weakened to the point of needing a ventilatory. Often triggered by infection, fever, adverse reaction to med.
Treatment myasthenia gravis
Cholinesterase inhibitors (stop breakdown of Ach, therefore increasing concentration in neuromuscular junction) *can result in cholinergic crisis that mimics myasthenic crisis, but problem is too much Ach instead of not enough (diarrhea, cramping, bradycardia, pupils constrict, increased salivation, risk for resp arrest)
What NT is involved in myasthenia gravis
Acetylcholine (the receptors (nicotinic receptors) in post synaptic side of the neuromuscular junction are destroyed :(
What is restless leg syndrome?
Neuro disorder characterized by unpleasant sensation in legs accompanied by urge to move legs, esp at bedtime
Risk factors restless leg
DM, ESRD, anemia, iron deficiency anemia, MS, PD, pregnancy, venous insufficiency
Time course restless leg
Worse at evening/ night time/ with rest, preventing sleep
Patho restless leg
Cause unknown- believed to involve genetic component, dysfunctional dopaminergic transmission, and low brain iron stores
Signs and symptoms restless leg syndrome
-Occur when the limbs are at rest and are relieved by movement
-Symptoms may extend to arms and trunk
-Commonly bilateral and symmetrical, but can be unilateral on occasion
-Sensation described as burning, nagging, aching, painful, itching bones, electric current, creepy crawl
Diagnosis of restless leg syndrome
does NOT require a sleep study
All of the following required: urge to move the legs, usually accompanied/ caused by unpleasant sensation in legs, symptoms begin or worsen during periods of rest of inactivity, symptoms are partially/ totally relived by movt, symptoms wose during evening/ night, symptoms cannot be due to another medical condition (i.e., arthritis)
positive supportive features: response to dopamine therapy
Treatment restless leg syndrome
Non pharm (sleep hygiene, hot baths, exercise moderately- yoga helps, massage, dc meds that can contribute (antidepressants, antiemetics, antihistamines, antipsychotics), avoid sleep deprivation
pharm: replace iron if deficient, dopaminergic agents, benzos, opioids, anticonvulsants, alpha 2 agonists
Describe the course and innervation of the median nerve
Arises from lateral and medial cords of brachial plexus, enters arm at axilla, travels with brachial artery down shaft of humerus into the cubital fossa, travels on ventral surface of forearm, passes through wrist through carpal tunnel (under the transverse carpal ligament) to hand.
Innervates all the muscles of the forearm anterior compartment (wrist and finger flexors, forearm pronators), ventral surface of thumb, 1st/ 2nd digit, half of 3rd digit
Most common cause of median nerve injury
carpal tunnel syndrome
What is carpal tunnel syndrome?
Median nerve become compressed in the carap tunnel (Osseo fascial tunnel composed of carpal bones and flexor retinaculum (fascia) due to swelling of tendons in the tunnel. Often caused by repetitive movements related to wrist flexion/ extension, holding wrist in awkward position, or strong gripping of objects
Signs and symptoms of carpal tunnel syndrome
- Tingling and numbness of the thumb, index, middle and ring fingers.
- Can also cause pain in the wrist with numbness/tingling
- Typically, the patient wakes at night with burning or aching pain and with numbness and tingling and shakes the hand to obtain relief and restore sensation.
- Long term compression leads to thenar muscle atrophy and weakness of the thumb and index fingers (can lead to hand of benediction- inability to flex middle and index finger)
Treatment of carpal tunnel
splinting, treat any underlying disorders contributing to inflammation, corticosteroid injection, surgical decompression
Describe two tests to support diagnosis of carpal tunnel
Tinel’s sign: lightly tapping on the ventral wrist over the median nerve elicits sensation of tingling/ pins and needles in the distribution of the nerve. Sensitivity 25-75%; specificity 70-90%.
Phalen’ maneuver: bring arms to shoulder level, bring back of hands together in midline, hold wrist in forced flexion for 30-60 seconds. Positive if tingling and numbness over median nerve distribution. Sensitivity 51-91%, specificity 33-88%
What is the most common compression neuropathy?
Carpal tunnel syndrome (followed by cubital- compression of ulnar nerve)
Describe the course and innervation of the radial nerve
Originates from brachial plexus, runs down radial groove of humerus to radial side of elbow, passes through supinator muscle, runs down middle of posterior forearm to dorsal thumb, 1st and 2nd digit.
Innervates extensors of the forearm, wrist, fingers, and thumb
What kind of injuries is the radial nerve susceptible to?
Entrapment can occur due to overuse injuries (most common pronation/ supination of wrist/ forearm)
Vulnerable to humeral mid shaft fracture
Can also sustain injury from improperly fitted crutches, shoulder dislocations, arm compression injuries
Can lead to wrist drop
Describe the course and innervation of the ulnar nerve
Down arm, passes posterior to medial epicondyle of humerus, travels along medial aspect of forearm, passes through the cubital tunnel at the wrist beneath the ulnar collateral ligament to the 4th/ 5th digit
Innervates flexors carpi ulnaris and most of intrinsic hand muscles. Sensation for 4th and 5th digits.
When you hit your funny bone, what nerve do you injure?
Ulnar
What is cubital tunnel syndrome
Compression/ traction of the ulnar nerve as it passes beneath the ulnar collateral ligament and between the two heads of the flexor carpi ulnaris muscle.
Where is the cubital tunnel?
Posterior aspect of elbow. Fibro-osseous tunnel.
Causes of cubital tunnel syndrome?
Leaning on the elbow, prolonged and excessive elbow flexion
Signs and symptoms of cubital tunnel
- Numbness and tingling along the ring and little fingers, and ulnar aspect of the hand
- Can present as elbow pain
- Long term compression causes weakness of intrinsic muscle of the hand and flexors of the ring and little finger
- Chronic compression leads to ulnar hand claw due to muscle imbalances (see picture below). An ulnar claw hand is metacarpophalangeal joint extension and interphalangeal joint flexion of the small and ring fingers caused by an imbalance between intrinsic and extrinsic hand muscles
What cranial nerve is CV VII?
Facial
What is cranial nerve VIII
Vestibulocochlear
What is cranial nerve IX
Glossopharangeal
Function of CV VII (facial)
Motor and sensory
- Facial expressions
- Supplies motor fibres to Lacrimal (tears) and salivary glands
- Taste (carries sensory fibres from taste buds of anterior part of tongue
Fx of CN VII (vestibulocochlear)
Sensory only
- Transmits sense of equilibrium (vestibular branch)
- Transmits sense of hearing (cochlear branch)
Fx of CN VIII (glossopharangeal)
Motor and sensory
- Motor fibres serve pharynx and salivary glands (gag and swallow reflex)
- Carries signals from pharynx, posterior tongue (taste) and pressure receptors of carotid artery
Cranial nerve VII (facial) dysfunction leads to what condition?
Bell’s Palsy
What is bell’s palsy? Unilateral or bilateral?
Unilateral facial nerve palsy (weakness or paralysis)
What causes Bell’s Palsy?
Exact etiology unknown, likely caused by inflammation of CNVII causing compression (CNVII travels through narrow canals in temporal bone and exits via the stylomastoid foramen).
May be due to reactivation of HSV in CNVII, or due to an autoimmune response.
Inflammation/ compression of CNVII leads to ischemia and degeneration, resulting in impaired signalling and transmission of motor impulses. Ipsilateral weakness or facial paralysis will result (along with loss of sensation in anterior tongue)
T/F With Bell’s Palsy, you will still see forehead wrinkling
False - this is impaired (unlike in stroke)
Risk factors for bell’s palsy
-Previous herpes simplex or herpes zoster infection, recent infection, diabetes, pregnancy (especially 3rd trimester), family history of Bell’s Palsy, hypertension, and hypothyroidism
Where do the Upper Motor Neurons arise?
Arise in the cerebral cortex
CN VII: where does it originate. How many branches does it contain?
CNVII originates in the Pons and runs through a narrow foramen of the temporal bone, out the stylomastoid foramen, through the parotid, and divides into 5 branches in the face (temporal, zygomatic, buccal, marginal mandibular, cervical)
Is onset of bell’s palsy slow or fast? How long does it take to resolve?
-Acute onset, progressing over hours to days
-Recovery in 3-4 weeks; may take up to 6 months (faster recovery occurs in mild/ moderate cases)
-Complete recovery in 80% of cases; without treatment, 70% of patients with complete and 94% with incomplete paralysis recover facial function in 6 months
What are the two tracts that upper motor neurons travel? Outline the path the signals travel on both tracts
Corticospinal – transports signals from cerebral cortex to lower motor neurons
Corticobulbar – transports signals from cerebral cortex to synapse with cranial nerve motor nuclei in the pons and medulla
S&S of bell’s palsy. Is it painful?
- Impaired forehead wrinkling
- Inability to close eye of affected side, drooping of eyelid
- Mouth drooping to affected side/ inability to smile
- Flattened nasolabial fold
- Can be associated with involuntary movements (synkinesis)
-Facial paresthesia
-Drooling
-Decreased tearing or abnormal lacrimation with eating
-Hypersensitivity to sound (hyperacusis)
-Ear pain
-Vesicular rash in ear (suggestive of Herpes Zoster cause and potential Ramsay-Hunt syndrome)
-Pain associated with facial palsy
-Change in sensation of taste (anterior tongue)
Is CT routine for bell’s palsy? WHen might we want one?
CT or MRI only if atypical presentation or physical findings suggestive of central lesion (affecting other cranial nerves, associated with limb weakness or ataxia), progressing paralysis, or lack of resolution
Meds used for bell’s palsy
Prednisone
Antivirals if severe
Eye drops
Acetaminophen
The corticospinal and corticobulbar tracts are the pyramidal tracts. What is the main function of the pyramidal system?
Allow for voluntary movements
In both types of pyramidal tracts some neurons decussate (crossover) to the contralateral side, while others stay ipsilateral. What percentage decussate in corticospinal and corticobulbar tracts?
Corticospinal:
Approximately 90% of neurons decussate (crossover) to contralateral side – known as lateral corticospinal tract in the white matter of the spinal cord
Approximately 10% of neurons stay ipsilateral and make up the anterior corticospinal tract
Corticobulbar:
50% of neurons synapse with lower motor neurons on ipsilateral side
50% decussate and synapse with lower motor neurons on the contralateral side
Where do lower motor neurons originate?
In the ventral horn grey matter of the spinal cord
What do lower motor neurons do?
Transport signals from the upper motor neuron to effector muscle to perform a movement
Use acetylcholine as their neurotransmitter
What is the neurotransmitter used by lower motor neurons?
Acetylcholine – binds with nicotinic cholinergic receptors on skeletal muscles resulting in muscle contraction
An upper motor neuron lesion can occur where? What are some possible causes?
result of damage to descending motor pathway at cortical, brainstem, or spinal cord levels
neoplasm, trauma, inflammation, cerebral palsy, MS, CVA, Parkinson’s
What muscle tone occurs with UMN leisons?
Muscle overactivity, Hypertonia/spasticity
In spinal shock- flaccid paralysis occurs for transient period followed by increased muscle tone particularly in antigravity muscles.
Describe involuntary movements associated with UMN lesions
Absence of involuntary movement
Clonus/spasm - occurs often due to loss of higher motor center control
Describe reflexes with UMN lesions
Reflexes can be hyperactive
Plantar reflex present
Describe muscle weakness with UMN lesions
Muscle groups affected, mild weakness, minimal disuse muscle atrophy.
A LMN lesion can occur where? What are some possible causes?
LMN are in anterior/ventral horn of spinal cord and motor nuclei of brainstem. Axon from these cell bodies bring impulses from UMN to skeletal muscles through anterior spinal roots or cranial nerves.
palsies, poliomyelitis, motor system disease, polyneuritis, muscular dystrophy, myasthenia gravis, polymyositis.
What muscle tone occurs with LMN lesions?
Hypotonia
Flaccidity
Describe involuntary movements associated with LMN lesions
fasciculations
Describe reflexes with LMN lesions
Hyporeflexia/areflexia Decreased muscle stretch reflexes
Absent plantar reflexes
Describe muscle weakness with LMN lesions
Individual muscles may be affected, mild weakness, marked muscle atrophy.
Can be asymmetrical and may involve one limb in beginning to become generalized with disease progression.
RECAP – compare and contrast UMN and LMN lesions
UMN
UMN syndromes are the result of damage to descending motor pathways at cortical, brainstem, or spinal cord levels
UMNs descend to the brainstem and decussate at the medullar pyramids to influence muscles on the contralateral side of the body
Clinical manifestations reflect muscle overactivity
UMN lesion (muscular) symptoms include:
Many affected muscles (all muscles at/below the lesion are affected)
Muscle weakness (can include spastic paresis/paralysis)
Hypertonia
Minimal muscle atrophy
Absence of involuntary movement
Clonus/spasms
LMN
LMNs have cell bodies in the ventral horn of the grey matter in the spinal cord. The axons exit via the ventral root and then synapse to a skeletal muscle
LMN syndromes impair both voluntary and involuntary movement.
The degree of paralysis or paresis is proportional to the number of LMNs affected
LMN lesion (muscular) symptoms include:
Limited number of muscles affected compared to UMN (think myotomes)
Muscle weakness (can include flaccid paresis/paralysis)
Hypotonia
Prominent muscle atrophy
Fasciculation (quivering of muscles of under the skin)
What is the most diagnosed sleep disorder?
Obstructive Sleep Apnea (OSA)
What are risk factors for OSA?
Obesity
Male gender
Older age
OSA is caused by blockage of the upper airways, what are some pathologies which can cause this blockage?
Allergies- cause swelling in the tissues of the nasopharynx
Swollen adenoids/tonsils – due to infection
Overbite – pulls jaw back and blocks the airway
Overweight/obesity – too much weight in the soft tissues of the neck which can weigh down the airway, especially when lying down.
The above are made worse by hormonal changes at night – causes the muscles around the airway to become slightly less stiff while sleeping, less able to keep the airway open and can become obstructed.
There is another type of sleep apnea called Central Sleep Apnea. What is the patho behind this form?
Refers to the fact that the problem stems from the CNS
Brain intermittently stops making an effort to breathe for 10-30 seconds
Apnea can persist for several seconds even after waking which can cause feelings of panic and further disrupt the sleep cycle
The respiratory system goes rapidly between no effort to breathe and hyperventilating with no in-between.
What might a person with OSA demonstrate for signs and symptoms while sleeping?
Excessive loud snoring
Gasping
Multiple apneic episodes (temporary pause of breathing) that lasts 10 seconds or longer
This periodic breathing eventually produces arousal out of sleep, resulting in decreased total sleep time and sleep and REM deprivation.
What are the daytime and long-term effects of OSA?
OSAS leads to hypercapnia and decreased O2 -> eventually leads to polycythemia, pulmonary hypertension, systemic hypertension, stroke, right-sided heart failure, dysrhythmias, liver congestion, cyanosis, and peripheral edema.
Hypersomnia (excessive daytime sleepiness) – can be severe, may fall asleep while talking, working, driving.
Impaired mood and cognitive function; symptoms include impairment of attention, episodic memory, working memory, and executive functions.
Outline diagnostics for OSA
As per the BC Practice Guidelines: A Home Sleep Assessment Test (HSAT) is used first in symptomatic patients only. If that is negative/inconclusive, then a polysomnography is recommended.
(Polysomnography records your brain waves, the oxygen level in your blood, heart rate and breathing, as well as eye and leg movements during the study.)
What does treatment look like for OSA?
CPAP, dental devices, surgery of upper airway and jaw if indicated, and obesity management
Seizures can be focal or generalized, what is the difference?
A focal (or partial) seizure involves only one portion of the brain, either the left or right cerebral hemisphere. Can be simple or complex
A generalized seizure shows EEG changes in both hemispheres of the brain. Almost always involve loss/impaired consciousness
What are some shared findings of both simple and complex focal seizures?
Partial (focal) seizures generally only involve one portion of the brain (either left or right cerebral hemisphere)
most common type of seizure
May be accompanied by visual or auditory hallucinations
Aura is common
Focal seizures can be classified as Simple Partial Seizures (SPS) or Complex Partial Seizures (CPS), what is the main difference?
Complex seizures are notable for impaired consciousness. Complex also may be followed by confusion, fatigue, headaches.
SPS common symptoms include jerking of a limb and may be preceded by an aura, including epigastric discomfort, fear, or unpleasant smells
Generalized seizures typically involve loss/impairment of consciousness and may be preceded by an aura. List the 4 subtypes of generalised seizures
Tonic-clonic (grand mal) seizures
Absent Seizures (petit mal)
Atonic Seizures (drop seizures)
Myoclonic Seizures
What are some findings and considerations for Tonic-clonic seizures?
Generally last one to two minutes
Notable for falls, cries, rigidity (tonicity), jerking (clonicity), with possible cyanosis, and urinary incontinence.
May be preceded by a prodome of unease or irritability (hours or days).
A grand mal seizure is followed by a postictal phase.
What are some findings and considerations for Absence seizures?
Usually last 2 to 15 seconds
Notable for beginning and ending abruptly.
Symptoms noted include staring, eye flutters or eye rolling, and automatisms.
First aid is not required.
What are some findings and considerations for atonic seizures?
Characterized by abrupt loss of muscle tone, loss of posture, or sudden collapse.
These seizures tend to be resistant to medication.
Protective headgear may be needed.
Generally first aid is not required unless an injury occurs.
What are some findings and considerations for myoclonic seizures?
Characterized by rapid, brief contraction of muscles (sudden jerks or clumsiness), usually on both sides of the body, arm, or sudden jerk of a foot during sleep.
First aid is generally not required.
A single spasm upon transition to sleep is considered normal.
What is Status Epilepticus?
A state of continuous seizures lasting more than 5 minutes, or rapidly recurring seizures without regaining consciousness from previous seizure or a single seizure lasting more than 30 minutes
Phases of a seizure include the preictal, ictal and postictal phases. Outline these phases
Preictal – includes prodroma(early clinical manifestations such as malaise, headache and depression which may occur days to hours before onset of a seizure) and aura (gustatory, visual or auditory experience or a feeling of dizziness or numbess)
Ictal – includes tonic phase (state of muscle contraction with excessive muscle tone) and clonic phase (state of alternating contraction and relaxation of muscles)
Post-ictal – time immediately following seizure, may experience headache, confusion, memory loss, dysphagia, and paralysis that can last hours-2 days. Deep sleep is common
Who is most likely to get Parkinson’s Disease?
Primary PD begins after age 40, increasing incidence after age 60
More prevalent in males
Describe the patho of Parkinson’s. Which neurotransmitter is involved?
Degeneration of basal ganglia with dysfunctional alpha-synuclein protein and loss of dopamine producing neurons in substantia nigra and dorsal striatum
Depletion of dopamine and excess of cholinergic activity in the feedback circuit
True or false – Parkinson’s disease is curable
False – chronic and incurable. A progressive condition with worsening symptoms over time.
No therapies are effective for slowing or stopping brain degeneration in PD
What will you see for motor impairments in Parkinson’s?
Temor – most notable in hands, “pill rolling tremor”, a resting tremor which diminishes with movement
Rigidity – stiffness, can see “cogwheel rigidity” where there are series of catches or stalls was a person’s limb is passively moved. Postural changes – stooped. Stare – expressionless face.
Akinesia (absence of movement) /bradykinesia (slow movement) /hypokinesia (lessened movement). All three involve difficulty initiating movement. Create shuffling gait, small steps.
Postural instability – poor balance, can lead to falls
What will you see for non-motor impairments in Parkinson’s?
Psychiatric: Cognitive impairment, Depression, anxiety, Sleep difficulties → wild dreams, Mood disturbances, Decreased motor learning ability, Dementia (advanced stages)
Micrographia
Autonomic dysfunction: Orthostatic hypotension, Constipation, Increased sweating
Decreased sense of smell
What are some complications of Parkinson’s?
Freezing phenomenon: Progressive hypokinesia, bradykinesia → akinetic pause in movement
Falls
Dystonia – involuntary muscle contractions leading to disfiguring and painful postures
Dementia - Common after prolonged, primarily motor disease
True or false: Parkinson’s disease causes muscle weakness
Despite the various motor symptoms of PD, there is no weakness of muscles. This differentiates PD from motor cortex or corticospinal pathway diseases.
How is Parkinson’s diagnosed?
There is no definitive diagnostic test for PD. Thus, dx is based on clinical presentation.
Parkinsons should be suspected in anyone with tremor, stiffness, slowness, balance problems, or gait disorders.
CT or MRI brain scanning should not be routinely used to diagnose PD
Patients, especially young, who request genetic testing should be assessed by a movement disorder specialist.
Clinical presentation
Resting tremor, rigidity, bradykinesia
Dopaminergic medication response
Dizziness and vertigo could be a sign of dysfunction of which cranial nerve?
Vestibulocochlear (VIII)
A loss of gag reflex is reflective of dysfunction in what cranial nerve?
IX (glossopharangeal)
Compare cranial nerves IX (glossopharangeal) and XII (hypoglossal)
Glossopharangeal: both motor and sensory. M: pharynx and salivary glands, responsible for gag and swallow. S: taste from posterior tongue and pressure receptors of carotid artery.
Hypoglossal: motor only. Responsible for muscles required in speech and swallowing.
So both are involved in motor component of swallowing.
Motor syndromes in what part of the brain are associated with ataxia and other symptoms of uncoordinated movement?
Cerebellum
T/F Damage to the right side of the cerebellum generally causes symptoms on the right side of the body
TRUE. Cerebellar motor syndromes primarily influence the same side of the body; for example, damage to the
right cerebellum generally causes symptoms on the right side of the body
What is the term for: Impairment of the ability to make movements exhibiting a rapid change of motion that is caused by cerebellar dysfunction
Dysdiadokokinesis
Which part of the brain controls fine motor movements?
Cerebellum
(also posture, balance and motor learning)
What neurological disorder can have cerebellar and corticospinal involvement that presents as nystagmus, ataxia, and weakness with all four limbs involved?
(there may be multiple but this one stands out in the ILOs…. just trying to figure out what cerebellar disorders Don wants us to know!)
MS
What kind of somatory sensory receptors are responsible for touch and proprioception?
Mechanoreceptors
What kind of somatic sensory receptors transmit pain?
Nociceptors
What kind of somatic sensory receptors transmit temperature?
Thermoreceptors
Which types of somatosensory fibres are nonmyelinated?
Type C
What stimuli do type C fibres sense?
- Sense burning pain and hot temperatures
- dull, aching, throbbing, and poorly
localized pain - visceral pain (tends to be poorly localized with an aching,
gnawing, throbbing, or intermittent cramping quality)
What stimuli do type A fibres sense? Differentiate Type A alpha and beta from delta
Type A delta – sharp pain, gross touch, cold temp
type A alpha, A beta – fastest fibers, proprioception, vibration, fine touch
Overall: type A fibres conduct SHARP PAIN, TOUCH, COLD TEMP, VIBRATIONS, and PROPRIOCEPTION
Differentiate the spinothalamic tract (a somatosensory tract) in terms of what signals are transmitted via the lateral and anterior tracts
Lateral tract = sensory information for pain and temperature
Anterior tract = sensory information for touch and pressure.
(osmosis says everything but crude touch is lateral…. mixed messages!)
T/F A fibres are myelinated
True
What are the 2 tracts of the somatosensory system?
1) Medial Lemniscal Pathway
2) Spinothalamic tract
Which neurodegenerative disease affects both upper and lower motor neurons?
ALS
What is ALS?
= a worldwide neuro-degenerative disorder that
diffusely involves lower and upper motor neurons, resulting in progressive muscle weakness
Amyotrophic (without muscle nutrition or progressive muscle wasting) refers to the predominant lower
motor neuron component of the syndrome. Lateral sclerosis, scarring of the corticospinal tract in the lateral
column of the spinal cord, refers to the upper motor neuron component of the syndrome.
Who is diagnosed with ALS?
ALS occurs in young adults or older adults, but it is most commonly diagnosed in middle to late
adulthood.
It affects both men and women
What causes ALS? Basic patho
We don’t know the cause.
- genetic associations
- very complex patho suggested involving abnormal genes, protein accumulation, inflammatory responses…all leads to motor neurons death
- motor neurons gradually break down and die –> brain can’t communicate so muscles become weak
S&S of ALS. How does it progress?
- initial symptoms are heterogeneous and can relate to UMN or LMN….about 60% have focal muscle weakness beginning in arms and legs and progressing to muscle atrophy, spasticity, and loss of manual dexterity and gait.
- Often starts with hand weakness, dropping things, tripping, cramping of upper extremities
- dysphagia
- dysarthria (muscles involved in speaking are weak)
- slurred or “thick” voice/dysphonia (poor voice quality)
- weakness and fasciculations
- inability to ambulate
- respiratory weakness/failure is late symptom
- recurrent pneumonias
- NO associated mental, sensory, or autonomic symptoms present.
What are the types of ALS? Which is most common? What percentage have a hereditary version?
Sporadic ALS - most common form of ALS
- The disease can affect anyone regardless of gender, ethnicity or age, although it most often affects people between the ages of 40 and 60.
- Children of those with sporadic ALS have no greater likelihood of developing ALS than the rest of the population.
Familial ALS
-Capable of being passed from a parent to his or her child.
- Approximately 5 to 10% of ALS cases are familial.
Bulbar ALS
- Regardless of whether someone has sporadic or familial ALS, 30% of all people with the disease have Bulbar ALS.
- In the early stages of Bulbar ALS, the motor neurons in the corticobulbar area of the brainstem are the first to be affected.
- This means that the muscles of the head, face and neck become paralyzed before muscles in other parts of the body.
What causes death in ALS?
Resp failure
ALS: average survival from onset to death _____years
3-5 years :(
T/F ALS isn’t associated with sensory deficits.
True! Only motor.
What would be an expected finding of dysfunction of CN I (Olfactory nerve)?
Usually due to trauma or a tumour.
Inability to detect smell.
What would be an expected finding of dysfunction of CN II (Optic nerve)?
Usually due to trauma, tumour, MS or stroke.
Blindness of a visual field defect.
What would be an expected finding of dysfunction of CN III (Oculomotor nerve)?
Usually due to diabetes or increased ICP.
Ptosis, dilated pupil.
Define migraine headache (without aura).
Migraine is an episodic neurological disorder characterized by a headache lasting 4 to 72 hours.
Migraine headache (without aura) is diagnosed when 2 of the following occur:
-unilateral throbbing head pain,
-pain worsens with activity,
-moderate or severe pain intensity;
+ and at least one of the following:
-nausea and/or vomiting
-photophobia and phonophobia
Persons with migraines have increased risk for developing which disorders?
Epilepsy
Depression & anxiety disorders
Cardiovascular disease
Stroke
What are the most common migraine headache triggers?
Too tired or oversleeping
Missed meals
Overexertion
Weather changes
Stress… or relaxation from stress (omg the poor person!)
Hormonal changes (mensturation)
Excess afferent stimulation (eg bright lights, strong smells)
Chemicals (alcohol, nitrates)
What are the 4 clinical phases of a migraine headache attack?
-Big flashcard, sorry. Hope it doesn’t trigger a migraine ;)
- Premonitory phase: ⅓ of persons have premonitory symptoms hours to days before onset of headache. Symptoms include: tiredness, irritability, loss of concentration, stiff neck, food cravings.
- Migraine aura: ⅓ of migraines come with aura symptoms at least some of the time; may last up to 1 hour. Aura symptoms can be visual, sensory, motor.
- Headache phase: throbbing pain usually begins on 1 side and spreads to include the entire head. HA may be accompanied by fatigue, N&V, dizziness. There may be hypersensitivity to anything touching the head. Symptoms last 4-72 hours (usually about 1 day).
- Recovery phase: irritability, fatigue, or depression; may take hours or days to resolve.
25-30% of migraines have aura.
What is aura?
Aura → experiencing strange smells, lights, visual disturbances, or even hallucinations before the onset of migraine
What are chronic migraines?
Begin as episodic migraines that increase in frequency over time.
Occurs at least 15 days in a month!!! …for more than 3 months
Can occur daily or on a near-daily basis.
What are chronic migraines associated with?
Overuse of analgesic migraine medications (sometimes called rebound headaches)
Obesity
Caffeine overuse.
Treatment: similar to that for episodic migraine.
Individuals with chronic migraine unresponsive to medical treatment should be evaluated for…?
Intracranial hypertension without papilledema and the possibility of sinus venous stenosis.
What is the pathophysiology of tension type headaches (TTH)?
Occur due to contraction of muscles of the scalp and neck
Predisposing factors:
-tension/stress
-cervical or back disorders
Episodic TTH: associated with peripheral pain mechanism-sensitization of myofascial sensory nerves
CTTH: associated with central pain mechanism- hypersensitivity of pain fibers from the trigeminal nerve that leads to central sensitization
What are the s/s of tension-type headache, or TTH?
-Mild to moderate bilateral headache with a sensation of a tight band or pressure around the head with onset of pain
-not aggravated by physical activity
-no other associated features
How do you diagnose CTTH?
Chronic Tension Type Headaches (CTTH): diagnosed when patient has TTH at least 15 days per month for at least 3 months
-need to rule out migraine or other types of headache
___________________ is a condition characterized by attacks of severe unilateral pain, accompanied by ipsilateral cranial autonomic symptoms and/or restlessness or agitation.
Cluster headache.
Describe some s/s of cluster headaches.
Cluster headaches are severe and sharp or stabbing in quality.
Pts are typically restless, prefer to pace about or sit and rock back and forth during an attack.
Symptoms most commonly occur in periorbital or temporal regions.
Cluster headache attacks are strictly unilateral, and the symptoms almost always remain on the same side of the head during a single attack.
Symptoms can switch to the other side during a different cluster attack (so-called side shift) in approx 15 percent of cases.
Autonomic symptoms typically occur only during the acute attack of cluster headaches. What presentations might you see?
Ipsilateral to the headache and may include ptosis, miosis, lacrimation, conjunctival injection, rhinorrhea, and/or nasal congestion. Sweating and increased cutaneous blood flow. Some report cutaneous allodynia.
Some patients with cluster have chronic signs of sympathetic paralysis such as miosis and ptosis that transiently intensify during acute attacks.
In rare cases, sympathetic disturbances persist on the previously affected side of the face in patients whose cluster headache has switched sides
Which imaging diagnostic is recommended for a patient with cluster headaches?
(MRI) of the brain with gadolinium for the initial evaluation of all patients with suspected cluster headache to exclude a structural abnormality of the brain and pituitary gland.
What are some treatment options for tension-type headache?
Mild: ice/heat for muscular tension
Mod-severe: NSAIDS, Acetaminophen, ASA, caffeine
Prevention strategies include
-stress reduction, daily exercise, massage, dental appliances for teeth grinding/clenching at night
CTTH: tricyclic antidepressants and behavioral/relaxation therapy
Botox injections are beneficial for some
Chronic tension-type headache (CTTH) is associated with which pain mechanism and cranial nerve?
Associated with central pain mechanism- hypersensitivity of pain fibers from the trigeminal nerve that leads to central sensitization.
What are some general physical characteristics on non-REM sleep?
Begins when the hypothalamus releases inhibitory signals.
Sympathetic tone decreases, and parasympathetic activities increase (remember rest and digest).
Men can experience penile erections; women can experience clitoral engorgement.
Basal metabolic rate decreases from 5-10%.
Pupil constriction occurs.
How many stages of non-REM sleep are there?
3
What are some characteristics of the
non-REM sleep stage N1?
What are some characteristics of the
non-REM sleep stage N1?
What are some characteristics of the
non-REM sleep stage N2?
Brain activity is still in theta (high frequency, low amplitude waves), but sleep spindles and K-complexes are seen on EEG.
Sleep spindles are brief bursts of high brain activity.
K-complexes are brief spikes in elevation of waves, quickly normalizes.
A theory behind spindles and K-complexes is that information is trying to process but the thalamus is filtering it out to help us remain asleep.
What are some characteristics of the
non-REM sleep stage N3?
Brain activity is delta waves (low frequency, high altitude waves).
Deep sleep, very difficult to wake from N3.
Growth hormones are released, cell repair is underway.
What are some characteristics of the Rapid Eye Movement (REM) sleep stage?
Brain activity resembles wakefulness, or theta in N1.
Most dreaming occurs in REM – these are the dreams we are most likely to remember.
AKA paradoxical sleep. The paradox is that we have a very active brain but also have muscle paralysis.
We can experience irregular heart rate, resp rate, and a change in body temperature.
This stage is important for memory and learning. If we learned something new that day and then did not have a great sleep with enough REM, we may have difficulty retaining that information.
The cycle typically cycles through
N1-> N2-> N3-> REM-> N1 or 2-> REM-> N1 or 2-> REM etc.
The first REM stage typically occurs after the first hour of sleep.
How many cycles of sleep are recommended, or ‘typical’ of a good night’s sleep?
4-6
Specific areas of the brain are responsible for different stages of our sleep cycle.
How does the hypothalamus influence sleep?
Hypothalamus: Major sleep centre. Secretes the neuropeptides acetylcholine and glutamate that promote wakefulness, and prostaglandin D2, adenosine, melatonin, serotonin, l-tryptophan, GABA and growth factors which promote sleep.
Specific areas of the brain are responsible for different stages of our sleep cycle.
How does the pontine reticular formation influence sleep?
Pontine reticular formation: Mainly responsible for creating REM sleep.
Specific areas of the brain are responsible for different stages of our sleep cycle.
How does the thalamocortical network influence sleep?
Thalamocortical network: Projections produce non-REM sleep.
Specific areas of the brain are responsible for different stages of our sleep cycle.
How do the pons and mesencephalon influence sleep?
Pons and Mesencephalon: Control REM sleep through REM-on and REM-off neurons.
Canada has one of the highest rates of multiple sclerosis (MS) in the world, with an estimated 90,000 Canadians living with the disease. On average, 12 Canadians are diagnosed with MS every day.
In what age range are most diagnoses made?
Most people are diagnosed with MS between the ages of 20 and 49 and the unpredictable effects of the disease will last for the rest of their lives.
MS is a chronic autoimmune disease of the central nervous system. Since that includes the brain, spinal cord and optic nerve, MS can affect which four functions?
MS can affect vision, memory, balance and mobility.
How does MS affect the nervous system?
The disease attacks myelin, the protective covering of the nerves, causing inflammation and often damaging the myelin. Myelin is necessary for the transmission of nerve impulses through nerve fibres. If damage to myelin is slight, nerve impulses travel with minor interruptions; however, if damage is substantial and if scar tissue replaces the myelin, nerve impulses may be completely disrupted, and the nerve fibres themselves can be damaged.
MS is unpredictable and may cause symptoms such as ?
Extreme fatigue
Lack of coordination
Weakness
Tingling
Impaired sensation
Vision problems
Bladder problems
Cognitive impairment
Mood changes
How is MS diagnosed?
Upon initial presentation of symptoms, refer to a neurologist.
Neuro will conduct a full medical history and a neurological examination to assess things like eye movement, strength and coordination. To reach a confirmed diagnosis of MS, the neurologist may employ additional tests, such as a Magnetic Resonance Imaging (MRI) scan which looks for tissue damage in the brain.
Is MS fatal? What is the expected prognosis
MS is not fatal for the vast majority of people living with the disease.
Most people who have MS can expect a normal or near-normal lifespan, thanks to improvements in symptom management and the MS disease-modifying therapies.
